Christopher R. Vakoc
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View article: Supplementary Figures S1-S17 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia
Supplementary Figures S1-S17 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia Open
Figures S1 to S17
View article: Supplementary Table 2 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia
Supplementary Table 2 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia Open
Supplementary Table 2
View article: Supplementary Table 1 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia
Supplementary Table 1 from SLC5A3-Dependent Myo-inositol Auxotrophy in Acute Myeloid Leukemia Open
Supplementary Table 1
View article: Key Resource Table 1 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies
Key Resource Table 1 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies Open
Key resource table
View article: Supplementary Tables S1-S5 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies
Supplementary Tables S1-S5 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies Open
Supplementary Table S1. Clinical sample information. Supplementary Table S2. Domain-focused sgRNA libraries used in this study and MAGeCK analysis of CRISPR screening results. Supplementary Table S3. sgRNA sequences. Supplementary Table S4…
View article: Supplementary Figures S1-S7 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies
Supplementary Figures S1-S7 from Systematic Evaluation of GAPs and GEFs Identifies a Targetable Dependency for Hematopoietic Malignancies Open
Supplemental Figure 1. Systematic domain-focused CRISPR screens of GAPs and GEFs and transcriptomic profiling identify ARHGAP45 as a hematologic malignancy-biased dependency linked to distinct genetic and risk subgroups. Supplemental Figur…
View article: A clinical-stage oncology compound selectively targets drug-resistant cancers
A clinical-stage oncology compound selectively targets drug-resistant cancers Open
Re-evaluating existing clinical compounds can uncover previously unrecognized mechanisms that reshape a drug's therapeutic potential. The small molecule Procaspase-Activating Compound 1 (PAC-1) entered oncology testing as a proposed activa…
View article: KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2
KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2 Open
Lineage plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and contributes to tumor heterogeneity and therapeutic resistance. Here, we identify KLF5 as a dynamic master regulator of epithelial lineage identity in PDAC, wit…
View article: Structural basis of DNA-dependent coactivator recruitment by the tuft cell master regulator POU2F3
Structural basis of DNA-dependent coactivator recruitment by the tuft cell master regulator POU2F3 Open
The transcription factor POU2F3 defines the identity of tuft cells and underlies a distinct molecular subtype of small cell lung cancer (SCLC). Although POU2F3 is considered undruggable, its activity critically depends on the coactivators …
View article: Correction: Targeting of epigenetic co-dependencies enhances anti-AML efficacy of Menin inhibitor in AML with MLL1-r or mutant NPM1
Correction: Targeting of epigenetic co-dependencies enhances anti-AML efficacy of Menin inhibitor in AML with MLL1-r or mutant NPM1 Open
View article: Abstract 1652 Structural and Functional Characterization on the SCP4-STK35 Phospho-Signaling Complex
Abstract 1652 Structural and Functional Characterization on the SCP4-STK35 Phospho-Signaling Complex Open
View article: Histone chaperones coupled to DNA replication and transcription control divergent chromatin elements to maintain cell fate
Histone chaperones coupled to DNA replication and transcription control divergent chromatin elements to maintain cell fate Open
The manipulation of DNA replication and transcription can be harnessed to control cell fate. Central to the regulation of these DNA-templated processes are histone chaperones, which in turn are emerging as cell fate regulators. Histone cha…
View article: PKM splice-switching ASOs induce upregulation of dual-specificity phosphatases and dephosphorylation of ERK1/2 in hepatocellular carcinoma
PKM splice-switching ASOs induce upregulation of dual-specificity phosphatases and dephosphorylation of ERK1/2 in hepatocellular carcinoma Open
Pyruvate kinase muscle isoform 2 (PKM2) is preferentially expressed in nearly all cancers. It primarily functions as the last enzyme in glycolysis but has other reported noncanonical functions, including recruiting transcription factors to…
View article: Supplementary Table S10A from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S10A from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
RNA-seq results. Combined tables for DESeq2 output of Ctrl, MARK2/3, YAP/TAZ double knockout in 20 cancer cell lines.
View article: Supplementary Figure S7 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Figure S7 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
A, IP–western blot analysis evaluating the interaction between 14-3-3e and YAPWT and YAP5D mutants or TAZWT and TAZ4D mutants in HEK-293T cells. Aspartate mutant reversion to wild-type S/T is indicated. Data are representative of two indep…
View article: Supplementary Table S5 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S5 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
P value for synergy score paralog combinations. Table of P value corresponding to synergy scores calculated using GEMINI.
View article: Supplementary Table S10B from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S10B from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
RNA-seq results. Combined tables for DESeq2 output of Ctrl, MARK2/3, YAP/TAZ double knockout in 20 cancer cell lines.
View article: Supplementary Table S2 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S2 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
Paralog CRISPR screening data 2. Table of calculated gene level log2(fold-changes) of Paralog
View article: Supplementary Table S3 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S3 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
Cancer cell line model information. Table of mutations and cancer driver of cell lines used in this study.
View article: Data from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Data from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
The Hippo signaling pathway is commonly dysregulated in human cancer, which leads to a powerful tumor dependency on the YAP/TAZ transcriptional coactivators. In this study, we used paralog cotargeting CRISPR screens to identify kinases MAR…
View article: Supplementary Figure S10 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Figure S10 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
A, Western blot analysis of YAP localization following doxycycline (Dox) induced empty vector control, MKIWT or MKIMUT expression for 24h in YAPC cells. Nuclear (Nuc) and cytosolic (Cyto) fractionation are indicated. (Data shown are an ext…
View article: Supplementary Table S1 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S1 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
Paralog CRISPR screening data. Table for sgRNA sequences and raw sequencing counts of paralog CRISPR screens in 22 cancer cell lines.
View article: Supplementary Table S6 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S6 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
FDR for synergy score paralog combinations. Table of FDR corresponding to synergy scores calculated using GEMINI.
View article: Supplementary Table S4 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S4 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
Synergy score paralog combinations. Table of synergy scores calculated using GEMINI.
View article: Supplementary Table S9 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S9 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
sgRNA sequences. Table of all sgRNA-sequences used in this study.
View article: Supplementary Figure S9 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Figure S9 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
A, Sanger sequencing Chromatogram of NF2 locus in MDA-MB231 cells. B, C, Rescue experiment of MARK2+3dKO in Cas9+ YAPC cells following knockout of indicated genes. Data shown are the mean ± SD of %GFP+ (normalized to day 3 after infection)…
View article: Supplementary Table S8 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S8 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
Phosphosite identification using mass spectrometry. Combined table of peptides identified using mass spectrometry.
View article: Supplementary Figure S8 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Figure S8 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
A, Rescue experiment of MARK2+3dKO in Cas9+ YAPC cells following knockout of indicated genes. Data shown are the mean ± SD of %GFP+ (normalized to day 3 after infection). n=3-6. P values are calculated using a mixed effects model (consider…
View article: Supplementary Table S11 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Table S11 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
YAP:TEAD4 bound YAP/TAZ dependent enhancers. Peak location file for enhancers with YAP,TEAD4 binding, and reduction of signal upon YAP/TAZ knockout.
View article: Supplementary Figure S1 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer
Supplementary Figure S1 from MARK2/MARK3 Kinases Are Catalytic Codependencies of YAP/TAZ in Human Cancer Open
A,B, CRISPR screening results from 22 cancer cell lines. A, Abundance fold-change of positive controls (dgRNAs targeting essential genes n=28 paired with control) and negative controls (dgRNAs targeting non-coding regions n=54 and nontarge…